Early markers of neural dysfunction and compensation: A model from minimal hepatic encephalopathy |
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| Affiliation: | 1. Department of General Psychology, University of Padua, Via Venezia 8, 35131 Padua, Italy;2. Department of Medicine, University of Padua, Via Giustiniani 2, 35128 Padua, Italy;3. CIRMANMEC, Via Giustiniani 2, 35128 Padua, Italy;4. Hepatobiliary Surgery, Department of Surgery, University of Padua, Via Giustiniani 2, 35128 Padua, Italy;1. Medicine & Rheumatology Unit, IRCCS Istituto Ortopedico Rizzoli, via Cesare Pupilli 1, 40136 Bologna, Italy;2. Radiology Unit, Department of Experimental, Diagnostic and Specialty Medicine, S. Orsola Malpighi University Hospital, via Giuseppe Massarenti 9, 40138 Bologna, Italy;3. Diagnostic and Interventional Radiology Unit, IRCCS Istituto Ortopedico Rizzoli, via Cesare Pupilli 1, 40136 Bologna, Italy;4. Department of Biomedical and Neuromotor sciences (DIBINEM), University of Bologna, via Giuseppe Massarenti 9, 40138 Bologna, Italy;1. Division of Gastroenterology and Hepatology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, United States;2. Division of Gastroenterology and Hepatology, University Hospital of Lausanne and University of Lausanne, Switzerland;1. Centro de Investigación Mente, Cerebro y Comportamiento, Universidad de Granada, Granada 18071, Spain;2. Departamento de Psicología Experimental, Universidad de Granada, Granada 18071, Spain;3. Dipartimento di Psicologia Generale. Università degli Studi di Padova, Padova 35100, Italy;4. Dipartimento di Neuroscienze: SNPSRR, Università degli Studi di Padova, Padova 35100, Italy;5. Centro di Neuroscienze Cognitive, University of Padua, Padova 35100, Italy;1. Department of Medicine, University of Padua, Italy;2. C.I.R.M.A.ME.C., University of Padua, Italy;3. IRCCS San Camillo, Lido di Venice, Italy;4. Department of Information Engineering, University of Padua, Italy;5. Department of General Psychology, University of Padua, Italy;1. Department of Hepatology, Postgraduate Institute of Medical Education & Research, Chandigarh 160012, India |
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| Abstract: | ObjectiveThe Inhibitory Control Task (ICT) was used to detect minimal hepatic encephalopathy (MHE). ICT assesses attention, working memory and inhibition by evaluating performance in detect, go and nogo trials, respectively. The event-related potentials (ERPs) elicited by the ICT provide insight into neural mechanisms underlying the cognitive alterations associated with MHE.MethodsThe performance and the ERPs elicited by ICT were measured in 31 patients with cirrhosis (13 with and 18 without MHE) and in 17 controls. The latency and amplitude of the N2, P3a, P3b and nogo-P3 were compared among the groups.ResultsPatients with MHE performed worse in all ICT trials compared to patients without MHE and controls. Cirrhotic patients, both with and without MHE, displayed a reduction in P3a amplitude, selectively in the detect trials. Patients without MHE exhibited greater N2 and nogo-P3 amplitudes compared to patients with MHE and controls.ConclusionsBoth patients with and without MHE displayed neural alterations reflecting attentional deficits (i.e., P3a attenuation). However, patients without MHE coped with such dysfunctions by recruiting compensatory neural mechanisms, as suggested by the enhancement of the nogo-P3 and N2 amplitudes coupled with a normal ICT performance.SignificanceThe study suggests how initial brain dysfunction might be compensated for by recruitment of additional neurocognitive resources. |
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| Keywords: | Event-related potentials Inhibition Compensation Minimal hepatic encephalopathy N2 P3 Cirrhosis |
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